Page 1345 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

918 PART 8: Renal and Metabolic Disorders

response to shock. Systemic hypoperfusion activates the sympathetic
TABLE 97-2 Causes of Acute Renal Failure
nervous system and renin-angiotensin-aldosterone axis. Norepinephrine
Prerenal and angiotensin II are systemic vasoconstrictors, and tend to increase
Volume depletion: Gastrointestinal fluid loss or hemorrhage; renal losses (diuretics or glu- renal blood flow by preserving renal perfusion pressure. On the other
cosuria, salt-wasting nephropathy, diabetes insipidus, or adrenal insufficiency); cutaneous hand, both hormones are renal vasoconstrictors, though they differ in
losses (burns, desquamation) their glomerular hemodynamic effects. Angiotensin II preferentially
Volume redistribution: Peripheral vasodilation (sepsis or antihypertensives), peritonitis, constricts efferent arterioles, and helps preserve glomerular filtration,
burns, pancreatitis, hypoalbuminemia (nephrotic syndrome or hepatic disease) increasing filtration fraction (the ratio of GFR to renal plasma flow) by
creating “back-pressure” to augment net filtration pressure in the glo-
Cardiac dysfunction: Pericardial tamponade, complications of myocardial infarction, acute merular capillary. Norepinephrine causes balanced afferent and efferent
or chronic valvular disease, cardiomyopathies, arrhythmias arteriolar constriction, similarly increasing filtration fraction in the face
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Vasodilatory shock: Sepsis, liver failure, postcardiotomy, anaphylaxis, or antihypertensives of decreased renal blood flow, but to a lesser extent than angiotensin II.
Renal vasoconstriction: Cirrhosis, sepsis, hypercalcemia, drugs (cyclosporine, tacrolimus, Both angiotensin II and norepinephrine stimulate intrarenal vasodilator
nonsteroidal anti-inflammatory drugs, or pressors) prostaglandin production, thus attenuating their simultaneous effect of
afferent arteriolar vasoconstriction and helping preserve renal perfusion.
Renal
Drugs may unfavorably alter the glomerular hemodynamic response
Ischemia: Trauma, surgery, sepsis, pigment nephropathy (hemolysis or rhabdomyolysis), to renal hypoperfusion. Nonsteroidal anti-inflammatory drug (NSAID)
cardiac or aortic hemorrhage administration to patients with decreased effective arterial blood
Nephrotoxic: Radiocontrast, antibiotics (aminoglycosides or amphotericin), nonsteroidal volume (due to hypovolemia or congestive heart failure) or renal vaso-
anti-inflammatory drugs, carbon tetrachloride, ethylene glycol, heavy metals (lead, constriction (due to cirrhosis) leads to a decline in renal blood flow and
mercury, arsenic, cadmium, or uranium), pesticides, fungicides, cyclosporine, or tacrolimus GFR. These patients are dependent on vasodilator prostaglandins to
maintain renal perfusion, so NSAIDs leave renal vasoconstrictor influ-
Disorders of glomeruli and blood vessels: Poststreptococcal glomerulonephritis, infective ences unopposed. Angiotensin-converting enzyme inhibitors (ACEIs)
endocarditis, systemic lupus erythematosus, Goodpasture syndrome, microscopic and angiotensin receptor blockers (ARBs) can lead to prerenal azotemia
polyarteritis, Wegener granulomatosis, Henoch-Schöunlein purpura, idiopathic rapidly in patients who are dependent on angiotensin II for maintenance of
progressive glomerulonephritis, polyarteritis nodosa, malignant hypertension, thrombotic GFR. This phenomenon is most commonly seen in patients receiving
microangiopathies (hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, ACEIs or ARBs in the presence of hypovolemia, bilateral renal artery
postpartum renal failure, or antiphospholipid syndrome), renal artery embolism, renal stenosis, or unilateral renal artery stenosis with a solitary kidney.
artery dissection, bilateral renal vein thrombosis, or abdominal compartment syndrome Prerenal azotemia also leads to avid renal tubular sodium and water
Acute interstitial nephritis: reabsorption throughout the nephron. Catecholamines and angiotensin II
Allergic: Semisynthetic penicillin analogues (eg, methicillin, ampicillin, or nafcillin), cepha- directly increase sodium transport and reabsorption in the proximal
losporins, rifampin, ciprofloxacin, cotrimoxazole, sulfonamides, thiazides, furosemide, and distal nephron. Efferent arteriolar constriction by angiotensin II and
allopurinol, phenytoin, tetracyclines, or warfarin increased filtration fraction simultaneously lead to decreased peritu-
bular capillary hydraulic pressure and increased peritubular capillary
Infectious: Streptococcal, staphylococcal, leptospirosis, infectious mononucleosis,
diphtheria, brucellosis, Legionnaire disease, toxoplasmosis, or cytomegalovirus oncotic pressure. The combination of high oncotic pressure and low
hydraulic pressure in peritubular capillaries increases sodium and
Infiltrative: Sarcoidosis, lymphoma, leukemia water absorption in the proximal tubule, a process termed glomerulo-
Autoimmune/alloimmune: Systemic lupus erythematosus or renal transplant rejection tubular balance. Angiotensin II also leads to downstream production
Postrenal of aldosterone, another salt-retaining influence. Severe hypovolemia/
hypotension (>10%-15% decrease in MAP or blood volume) leads to
Malignancy: Lymphoma, renal adenocarcinoma, bladder ureteral carcinoma, gynecologic nonosmotic vasopressin secretion, and avid water reabsorption in the
cancers, prostate cancer, other pelvic tumors, or metastatic disease collecting duct, along with systemic vasoconstriction. Finally, in hypo-
Inflammatory processes: Tuberculosis, inflammatory bowel disease, retroperitoneal abscess volemic patients, decreased atrial stretch downregulates production of
or fibrosis, postradiation therapy atrial natriuretic peptide, also favoring sodium retention (the opposite
Vascular diseases: Aortic aneurysm, renal artery aneurysm is true if renal hypoperfusion is caused by congestive heart failure). Thus
the combination of glomerulotubular balance and the tubular effects of
Papillary necrosis: Diabetes mellitus, sickle hemoglobinopathy, analgesic abuse, prosta- catecholamines, angiotensin II, aldosterone, and vasopressin mediate
glandin inhibition, or hepatic cirrhosis
the salt and water retention which is the hallmark of prerenal azotemia.
Intratubular: Uric acid, calcium phosphate, Bence Jones proteins, methotrexate, acyclovir, Accordingly, patients with prerenal azotemia tend to have oliguria, low
sulfonamide antibiotics, or indinavir urine sodium, and concentrated urine with a urine osmolality exceeding
Miscellaneous: Nephrolithiasis, ureteral ligation, retrograde pyelography with ureteral 500 mOsm/kg. Low urine sodium (and fractional excretion of sodium;
edema, neurogenic bladder, neuropathic ureteral dysfunction, or obstructed urinary catheter see below) and increased urine osmolality (with a high urine:plasma
creatinine ratio) are not seen in patients who have prerenal AKI due
to renal losses (ongoing diuretic therapy, salt-wasting nephropathies,
osmotic diuresis, adrenal insufficiency, and central or nephrogenic dia-
decreased renal blood flow, GFR, intravascular volume, or a combina- betes insipidus). Other common laboratory features of prerenal AKI are
tion of these), a vasodilatory signal is transduced to the corresponding increased serum BUN:creatinine ratio (caused by low tubular flow and
afferent arteriole (and vice versa if flow increases). Together, these increased urea reabsorption), decreased fractional excretion of urea (see
mechanisms autoregulate renal blood flow in the face of hypotension below), polycythemia/high serum albumin (hemoconcentration), mild
or hypertension. A third mechanism additionally helps autoregulate hypercalcemia, hyperuricemia, and acid-base abnormalities (metabolic
GFR. Increased renin secretion stimulated by hypotension/hypovolemia acidosis from diarrhea or shock or lactic acidosis; metabolic alkalosis
sensed in the afferent arteriole helps maintain GFR (but not renal blood from diuretics or vomiting). Hyponatremia may also be present,
flow) during hypotension, through the efferent arteriolar action of depending on abnormalities in water balance (see Chap. 99). The renal
angiotensin II (discussed further below). response to volume challenge or vasoactive drug initiation may also be
Of course, in addition to local autoregulation, systemic neurohor- used to determine the presence or absence of a reversible, “prerenal”
monal influences also play a prominent role in determining the renal etiology of AKI.

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